Masayuki Yamanouchi1,2,3,4, Kengo Furuichi5, Junichi Hoshino2,4, Tadashi Toyama5, Akinori Hara5, Miho Shimizu5, Keiichi Kinowaki6, Takeshi Fujii6, Kenichi Ohashi6,7, Yukio Yuzawa8, Hiroshi Kitamura9, Yoshiki Suzuki10, Hiroshi Sato11, Noriko Uesugi12, Satoshi Hisano12, Yoshihiko Ueda13, Shinichi Nishi14, Hitoshi Yokoyama15, Tomoya Nishino16, Kenichi Samejima17, Kentaro Kohagura18, Yugo Shibagaki19, Koki Mise20, Hirofumi Makino20, Seiichi Matsuo21, Yoshifumi Ubara3,4, Takashi Wada1,5. 1. Department of Nephrology and Laboratory Medicine, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Graduate School of Medical Sciences, Kanazawa University, Ishikawa, Japan m.yamanouchi@toranomon.gr.jp twada@m-kanazawa.jp. 2. Nephrology Center, Toranomon Hospital, Tokyo, Japan. 3. Nephrology Center, Toranomon Hospital Kajigaya, Kanagawa, Japan. 4. Okinaka Memorial Institute for Medical Research, Tokyo, Japan. 5. Division of Nephrology, Kanazawa University Hospital, Kanazawa, Japan. 6. Department of Pathology, Toranomon Hospital, Tokyo, Japan. 7. Department of Pathology, Yokohama City University Graduate School of Medicine, Kanagawa, Japan. 8. Department of Nephrology, Fujita Health University School of Medicine, Aichi, Japan. 9. Department of Pathology, Clinical Research Center, National Hospital Organization Chiba-East National Hospital, Chiba, Japan. 10. Health Administration Center, Niigata University, Niigata, Japan. 11. Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences, Miyagi, Japan. 12. Department of Pathology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan. 13. Department of Pathology, Dokkyo Medical University Saitama Medical Center, Saitama, Japan. 14. Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Hyogo, Japan. 15. Department of Nephrology, Kanazawa Medical University School of Medicine, Ishikawa, Japan. 16. Department of Nephrology, Nagasaki University Hospital, Nagasaki, Japan. 17. Department of Nephrology, Nara Medical University, Nara, Japan. 18. Department of Cardiovascular Medicine, Nephrology and Neurology, University of the Ryukyus School of Medicine, Okinawa, Japan. 19. Division of Nephrology, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan. 20. Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. 21. Division of Nephrology, Department of Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Abstract
OBJECTIVE: Clinicopathological characteristics, renal prognosis, and mortality in patients with type 2 diabetes and reduced renal function without overt proteinuria are scarce. RESEARCH DESIGN AND METHODS: We retrospectively assessed 526 patients with type 2 diabetes and reduced renal function (estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m2), who underwent clinical renal biopsy and had follow-up data, from Japan's nationwide multicenter renal biopsy registry. For comparative analyses, we derived one-to-two cohorts of those without proteinuria versus those with proteinuria using propensity score-matching methods addressing the imbalances of age, sex, diabetes duration, and baseline eGFR. The primary end point was progression of chronic kidney disease (CKD) defined as new-onset end-stage renal disease, decrease of eGFR by ≥50%, or doubling of serum creatinine. The secondary end point was all-cause mortality. RESULTS: Eighty-two patients with nonproteinuria (urine albumin-to-creatinine ratio [UACR] <300 mg/g) had lower systolic blood pressure and less severe pathological lesions compared with 164 propensity score-matched patients with proteinuria (UACR ≥300 mg/g). After a median follow-up of 1.9 years (interquartile range 0.9-5.0 years) from the date of renal biopsy, the 5-year CKD progression-free survival was 86.6% (95% CI 72.5-93.8) for the nonproteinuric group and 30.3% (95% CI 22.4-38.6) for the proteinuric group (log-rank test P < 0.001). The lower renal risk was consistent across all subgroup analyses. The all-cause mortality was also lower in the nonproteinuric group (log-rank test P = 0.005). CONCLUSIONS: Patients with nonproteinuric diabetic kidney disease had better-controlled blood pressure and fewer typical morphological changes and were at lower risk of CKD progression and all-cause mortality.
OBJECTIVE: Clinicopathological characteristics, renal prognosis, and mortality in patients with type 2 diabetes and reduced renal function without overt proteinuria are scarce. RESEARCH DESIGN AND METHODS: We retrospectively assessed 526 patients with type 2 diabetes and reduced renal function (estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m2), who underwent clinical renal biopsy and had follow-up data, from Japan's nationwide multicenter renal biopsy registry. For comparative analyses, we derived one-to-two cohorts of those without proteinuria versus those with proteinuria using propensity score-matching methods addressing the imbalances of age, sex, diabetes duration, and baseline eGFR. The primary end point was progression of chronic kidney disease (CKD) defined as new-onset end-stage renal disease, decrease of eGFR by ≥50%, or doubling of serum creatinine. The secondary end point was all-cause mortality. RESULTS: Eighty-two patients with nonproteinuria (urine albumin-to-creatinine ratio [UACR] <300 mg/g) had lower systolic blood pressure and less severe pathological lesions compared with 164 propensity score-matched patients with proteinuria (UACR ≥300 mg/g). After a median follow-up of 1.9 years (interquartile range 0.9-5.0 years) from the date of renal biopsy, the 5-year CKD progression-free survival was 86.6% (95% CI 72.5-93.8) for the nonproteinuric group and 30.3% (95% CI 22.4-38.6) for the proteinuric group (log-rank test P < 0.001). The lower renal risk was consistent across all subgroup analyses. The all-cause mortality was also lower in the nonproteinuric group (log-rank test P = 0.005). CONCLUSIONS:Patients with nonproteinuric diabetic kidney disease had better-controlled blood pressure and fewer typical morphological changes and were at lower risk of CKD progression and all-cause mortality.
Authors: Oyunchimeg Buyadaa; Dianna J Magliano; Agus Salim; Digsu N Koye; Jonathan E Shaw Journal: Diabetes Care Date: 2019-12-03 Impact factor: 19.112